Background: Peripheral muscle electrostimulation (PME), encompassing neuromuscular electrical stimulation (NMES) and functional electrical stimulation (FES), has been increasingly acknowledged as an effective adjunctive or complementary treatment to voluntary exercise in elderly cardiac patients who cannot perform sufficient amounts of exercise, for whom there is limited research on optimal protocols. Sarcopenia, defined as a progressive decrease in muscle mass, strength and function, affects approximately 34% of heart failure (HF) patients and considerably worsens their prognosis. The objective of this systematic review is to summarize current evidence on the theoretical mechanisms, physiological pathways, safety and efficacy of PME in older adults within a cardiac rehabilitation (CR) setting, with a specific emphasis on sarcopenia reversal. Methods: We performed a systematic review following the PRISMA 2020 guidelines. A systematic search was conducted on the PubMed, Embase, Cochrane Library, CINAHL and PEDro databases from inception until December 2025. We searched for randomized controlled trials (RCTs) and controlled clinical trials focusing on PME in patients with cardiac diseases aged 65 years or older. The main outcomes were physical function (assessed with the Short Physical Performance Battery SPPB and 6 min walk distance 6MWD), muscle strength, muscle mass and safety. The Cochrane Risk of Bias tool was used to evaluate the quality of the studies. Results: Eight studies were included, with 387 participants and a mean age between 78 and 85 years. PME consistently improved lower-extremity muscle strength (MD: 5.2% body weight, 95% CI = 1.2–9.1, p = 0.013) along with SPPB scores, which ranged from +2.3 to +2.67 points (all p < 0.05). Home-based PME (NMES) achieved 100% adherence rates, and no cardiovascular adverse events were reported. The mechanisms by which PME is beneficial involve peripheral skeletal muscle adaptations without eliciting central hemodynamic stress, increased endothelial function, aerobic enzyme activity, protein anabolism stimulation or muscle proteolysis inhibition. No significant effects were observed on BNP levels, hospital readmissions or mortality. PME has been shown to attenuate the progression of sarcopenia through hypertrophy of type I and II muscle fibers, as well as mitochondrial biogenesis. Conclusions: PME is a safe, feasible adjunct to conventional CR in frail, elderly cardiac patients, particularly those with exercise intolerance and sarcopenia. It improves peripheral muscle function, physical performance, and muscle protein balance without cardiovascular stress. Larger multicenter trials are needed to establish optimal protocols and long-term clinical outcomes.
Sendrowski et al. (2026) studied this question.